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SUMMARY OF RESEARCH
Impairment of intracellular trafficking resulting in mislocalization or accumulation of signaling molecules in the wrong compartment can have devastating physiological effects. In pathologies as systemic lupus erythematosus (SLE) defective intracellular signaling events in different cell types caused by altered receptor structure, modulation of membrane clustering, lipid-raft distribution of signaling molecules, and defective signal silencing mechanisms, play a key role in the chronic inflammatory process that perpetuates the disease. In this project we will focus our attention in two main objectives. First, in SLE patients we will study the alterations in several signaling events with special interest on identifying the subcellular organelles (Golgi or recycling endosomes) where CD38 signals immediately after CD38 engagement at the plasma membrane, the functional role of CD38 on the immunological synapse formation, and the role of CD38-associated lipid raft microdomains in this processes. Second, we will study the proteome of plasma or sera to identify biomarkers or biosignatures of human diseases with two major goals:
1) To know better the atherogenic pattern of patients with SLE and with other autoinmune diseases such as Systemic Sclerosis or Scleroderma.
2) To determine the response to specific pharmacological treatment these patients.
FUNDING AGENCIES LAST 5 YEARS
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-Martínez-Blanco, A.; Domínguez-Pantoja, M.; Botía-Sánchez, M.; Pérez-Cabrera, S.; Bello-Iglesias, N.; Carrillo-Rodríguez, P.; Martin-Morales, N.; Lario-Simón, A.; Pérez-Sánchez-Cañete, M.M.; Montosa-Hidalgo, L.; Guerrero-Fernández, S.; Longobardo-Polanco, V.M.; Redondo-Sánchez, S.; Cornet-Gomez, A.; Torres-Sáez, M.; Fernández-Ibáñez, A.; Terrón-Camero, L.; Andrés-León, E.; O¿Valle, F.; Merino, R.; Zubiaur, M.; Sancho, J., CD38 Deficiency Ameliorates Chronic Graft-Versus-Host Disease Murine Lupus via a B-Cell-Dependent Mechanism, Frontiers in Immunology, 2021, Vol. 12: 713697, ARTÍCULO, Id:854129 |
